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Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules
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Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules

Published on: May 12, 2017

Poliovirus unlinks TIA1 aggregation and mRNA stress granule formation

James P White1, Richard E Lloyd

  • 1Department of Molecular Virology and Microbiology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

Journal of Virology
|September 30, 2011
PubMed

Insights

Mammalian cells form stress granules (SGs) during stress, but poliovirus infection disrupts this process. Early SGs form, but later stages create pseudo-stress granules lacking key components.

Area of Science:

  • Cellular biology
  • Virology
  • Molecular biology

Background:

  • Mammalian cells form stress granules (SGs) containing translationally silenced messenger ribonucleoprotein complexes (mRNPs) in response to environmental stress and viral infection.
  • SGs are characterized as aggregates of stalled translation initiation complexes, including translation machinery and mRNA-binding proteins.

Purpose of the Study:

  • To investigate the dynamic formation and composition of stress granules during poliovirus infection.
  • To understand how poliovirus manipulates stress granule formation and function.

Main Methods:

  • Analysis of stress granule formation in poliovirus-infected cells under various stress conditions (viral infection, oxidative stress, heat shock, ER stress).
  • Immunofluorescence microscopy to visualize the localization of key proteins like TIA1 and translation initiation factors.
  • Expression of a modified RasGAP-SH3 domain binding protein to assess its impact on SG persistence.

Main Results:

  • Early poliovirus infection induces stress granules containing TIA1, translation factors, RNA-binding proteins, and mRNA.
  • As infection progresses, stress granule formation is blocked, resulting in pseudo-stress granules lacking translation initiation factors and mRNA.
  • These pseudo-SGs contain TIA1 but lack other defining SG components, a phenomenon observed across multiple stress types.

Conclusions:

  • Poliovirus infection severs the normal functions of TIA self-aggregation and stalled complex aggregation into stress granules.
  • This leads to the formation of novel foci containing TIA1 but lacking other essential stress granule components during late-stage infection.
  • Understanding this mechanism provides insight into viral strategies for host cell manipulation and potential targets for antiviral therapies.

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